Purpose: :
Endophthalmitis is a bacterial infection of the posteriorsegment of the eye that is either cleared by the host's immunesystem, or develops into a severe infection that destroys theeye. We previously demonstrated that C57BL/6J mice cleared a500 CFU intravitreal inoculation of Staphylococcus aureus, butC57BL/6J FasL–defective gld mice failed to clear an identicalinfection. Thus, C57BL/6J mice possessed a FasL–dependantresistance to destructive endophthalmitis. Interestingly, thereare two FasL allotypes expressed in mice; C57BL/6J mice expressFasL.1 and BALB/c mice express FasL.2. FasL.2 exhibits significantlygreater cytotoxic activity, indicating that the Fas/FasL systemworks more efficiently in FasL.2 mice. Given the importanceof FasL in resistance to endophthalmitis in C57BL/6J mice, wehypothesized that BALB/c mice, which express the stronger FasL.2allotype, would be more resistant to S. aureus–inducedendophthalmitis.

Results: :
Both C57BL/6J and BALB/c mice cleared 500 CFU of S.aureus, while 5000 CFU resulted in destructive endophthalmitis.Although both BALB/c and C57BL/6J mice cleared 2500 CFU of S.aureus, C57BL/6J mice demonstrated more extensive inflammationand retinal damage as compared to BALB/c mice. This indicatesthat BALB/c mice are more resistant to S. aureus endophthalmitis.To determine whether this increased resistance was due to FasL,BALB/c FasL knockout mice received a 500 CFU inoculation ofS. aureus. Unexpectedly, the loss of FasL did not eliminatethe host's resistance, and 83% of BALB/c FasL knockout micecleared the infection.

Conclusions: :
We conclude that BALB/c mice demonstrate increasedresistance to S. aureus, and that this resistance is independentof FasL. These data imply that other components of the innateimmune system are critical to BALB/c resistance to S. aureusendophthalmitis.